Unlike bacterial biofilms can be visible to the naked eye. As with many instances of bacteria they are often harmless to us but when the bacteria are dangerous the biofilm offers them protection (which is why they form such structures).

The term “biofilms” suggests a thin, two-dimensional substance, but these communities feature microscopic-scale tower-like structures crisscrossed with water channels, all of which is encased in a protective, self-produced slimy layer. The bacteria within communicate and demonstrate cooperative behavior reminiscent of primitive organs.
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According to the National Institutes of Health, more than 65 percent of chronic inflammatory and infectious diseases are due to biofilms. According to recent studies, biofilm-related infections claim as many lives as heart attack or cancer.
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Scientists think there are several reasons for this decrease in susceptibility. First, the slimy layer encasing biofilms can make it hard for disinfectants or antimicrobials to even physically reach the bacteria. Also, bacteria living in biofilms experience high stress levels while growing rather slowly, which can render most antibiotics ineffective since they only work on actively growing cells. My favorite theory is that living in a biofilm changes bacteria and their behavior; something about their mix of active genes and proteins just makes them more resilient. Whatever the contributing factors, bacteria growing in a biofilm can be up to 1,000-fold more resistant to antibiotics than the same bacteria grown planktonically.

The use of biofilms predates our use of anti-biotics but the adaptation of forming biofilm communities serves as a protection against antibiotics and so it isn’t a surprise that with more use of antibiotics more surviving bacteria will be those using biofilm strategies.

Controlling biofilms in the future will likely require a combination of strategies, addressing both attachment and escape, with and without the use of antibiotics and communication blockers, and likely in a manner more or less tailored toward the different bacterial lifestyles.

Thankfully for us, we have many researchers exploring options to help us figure out how we can protect ourselves when we need to. We are going to need many different strategies to protect us going forward. Our success will depended on thousands of scientists working on these issues.

I do also believe the wonderful breakthroughs we make when we invest in science and engineering have made our lives much better and have the potential to continue to do so in many ways, including in dealing with the risks of superbugs. But this is something that requires great effort by many smart people and a great deal of money. It will only happen if we put in the effort.

hey won this particular battle, or at least gained some critical intelligence, not by designing a new antibiotic, but by interfering with the metabolism of the bacterial “bugs” — E. coli in this case — and rendering them weaker in the face of existing antibiotics
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ROS, or “reactive oxygen species,” include molecules like superoxide and hydrogen peroxide that are natural byproducts of normal metabolic activity. Bacteria usually cope just fine with them, but too many can cause serious damage or even kill the cell. In fact, Collins’ team revealed a few years ago the true antibiotic modus operandi: they kill bacteria in part by ramping up ROS production.

We need to continue to pursue many paths to protecting us from rapidly evolving bacterial risks. Many promising research results will fail to produce usable solutions. We need to try many promising ideas to find useful tools and strategies to protect human health.

The human microbiome is a very interesting aspect of our health and biology.

The 99% figure they quote is mainly silly. It might be technically accurate, but it is much more misleading than accurate (if it is accurate). We have more non-human cells than human but those cells are much smaller and we are overwhelmingly made up of human cells by weight (95+%).

The complexity of healthy bodies is far from understood. It is interesting to watch our understanding of the balancing act going on inside of us. Many foreign “invaders” are critical to our health.

As concerns over deadly antibiotic-resistant strains of ‘superbug’ bacteria grow, scientists at the Salk Institute are offering a possible solution to the problem: ‘superhero’ bacteria that live in the gut and move to other parts of the body to alleviate life-threatening side effects caused by infections.

Salk researchers reported finding a strain of microbiome Escherichia coli bacteria in mice capable of improving the animals’ tolerance to infections of the lungs and intestines by preventing wasting–a common and potentially deadly loss of muscle tissue that occurs in serious infections. If a similarly protective strain is found in humans, it could offer a new avenue for countering muscle wasting, which afflicts patients suffering from sepsis and hospital-acquired infections, many of which are now antibiotic resistant.

Salk scientists found a strain of E. coli bacteria (left) that were able to stop muscle wasting in mice infected with either Salmonella Typhimurium (center) and Burkholderia thailandensis (right). Image courtesy the Salk Institute.

“Treatments for infection have long focused on eradicating the offending microbe, but what actually kills people aren’t the bacteria themselves–it’s the collateral damage it does to the body,” says Janelle Ayres, a Salk assistant professor in the Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis and senior researcher on the study.

“Our findings suggest that preventing the damage–in this case muscle wasting–can stave off the most life-threatening aspects of an infection,” she adds. “And by not trying the kill the pathogen, you’re not encouraging the evolution of the deadly antibiotic-resistant strains that are killing people around the world. We might be able to fight superbugs with ‘superhero’ bugs.”

Once the most powerful and revolutionary of drugs, antibiotics appear to have reached their limits, due to the ability of bacteria to rapidly evolve resistance to the medicines. The rise of antibiotic resistance presents a grave threat to people around the world, as diseases once easily controlled repel all attempts at treatment. A recent study found that up to half of the bacteria that cause infections in US hospitals after a surgery are resistant to standard antibiotics.

In the United States alone, two million people annually become infected with bacteria that are resistant to antibiotics and at least 23,000 people die each year as a direct result of these infections, according to the U.S. Centers for Disease Control.

The antibiotic, called teixobactin, kills a wide range of drug-resistant bacteria, including MRSA and bugs that cause TB and a host of other life-threatening infections.

It could become a powerful weapon in the battle against antimicrobial resistance, because it kills microbes by blocking their capacity to build their cell walls, making it extremely difficult for bacteria to evolve resistance.

It would be great if the exciting results carried through to real world results similar to the hope. Medical research is full of promising initial results that fail to deliver, however. We are at great risk if some new miracle anti-biotic isn’t found. Many people are investigating potential solutions.

Most antibiotics are isolated from bacteria or fungi that churn out lethal compounds to keep other microbes at bay. But scientists have checked only a tiny fraction of bugs for their ability to produce potential antibiotics because 99% cannot be grown in laboratories.

Lewis’s group found a way around the problem by developing a device called an iChip that cultures bacteria in their natural habitat. The device sandwiches the bugs between two permeable sheets. It is then pushed back into the ground where the microbes grow into colonies.
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Working with a Massachusetts-based company, NovoBiotic, and researchers at the University of Bonn, [Kim] Lewis’s group screened 10,000 soil bacteria for antibiotics and discovered 25 new compounds. Of these, teixobactin was the most promising.
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Though promising, Lewis said that years more work lie ahead before the drug could be available. Human clinical trials could begin within two years to check its safety and efficacy, but more development would follow that.

It is wonderful to read about the great work so many scientists are making in researching potential life saving drugs. Hopefully this antibiotic will save us from what will be catastrophic harm if some new antibiotic is not available soon.

Let’s say you get infected with a bacterium that causes annoying, but totally non-dangerous symptoms. If you just try to “live with it,” will your immune system eventually kill it, or does killing bacteria require antibiotics in all cases?

So your “existing” bacteria kill off others all the time too (you have lots of different types of bacteria full time in your body – they often settle into niches and fight off any others , which is normally good as they are long term residents your body has learned to live with them).

Also like everything bacteria die off themselves – though if the conditions are right they are multiplying like crazy so that exceeds die off.

People talk about genetics impact on getting cavities and impact of brushing and flossing well. Also the makeup of bacteria can help or hurt. If your mouth is home to certain bacteria tooth decay is less likely, home to others it is more likely. They tend to remain fairly steady (a certain makeup of bacteria will be consist for a person over the long term – not perfectly that way but tend that way). A UCLA microbiologist developed a mouthwash to try and ceed your mouth with good bacteria and oust the bad guys.

Raw honey has been used against infections for millennia, before honey – as we now know it – was manufactured and sold in stores. So what is the key to its’ antimicrobial properties? Researchers at Lund University in Sweden have identified a unique group of 13 lactic acid bacteria found in fresh honey, from the honey stomach of bees. The bacteria produce a myriad of active antimicrobial compounds.

These lactic acid bacteria have now been tested on severe human wound pathogens such as methicillin-resistant Staphylococcus aureus (MRSA), Pseudomonas aeruginosa and vancomycin-resistant Enterococcus (VRE), among others. When the lactic acid bacteria were applied to the pathogens in the laboratory, it counteracted all of them.

While the effect on human bacteria has only been tested in a lab environment thus far, the lactic acid bacteria has been applied directly to horses with persistent wounds. The LAB was mixed with honey and applied to ten horses; where the owners had tried several other methods to no avail. All of the horses’ wounds were healed by the mixture.

The researchers believe the secret to the strong results lie in the broad spectrum of active substances involved.

“Antibiotics are mostly one active substance, effective against only a narrow spectrum of bacteria. When used alive, these 13 lactic acid bacteria produce the right kind of antimicrobial compounds as needed, depending on the threat. It seems to have worked well for millions of years of protecting bees’ health and honey against other harmful microorganisms. However, since store-bought honey doesn’t contain the living lactic acid bacteria, many of its unique properties have been lost in recent times”, explains Tobias Olofsson.

This is a very cool: “When used alive, these 13 lactic acid bacteria produce the right kind of antimicrobial compounds as needed, depending on the threat.” As is the note that store bought honey doesn’t contain the living bacteria. My guess is some honey bought directly from farmers or bee-keepers, at farmer’s markets may well still have those live bacteria – but I am just guessing I may be wrong.

The next step is further studies to investigate wider clinical use against topical human infections as well as on animals.

The findings have implications for developing countries, where fresh honey is easily available, but also for Western countries where antibiotic resistance is seriously increasing.

Citing an overabundance in the use of antibiotics by the agriculture and aquaculture industries that poses a threat to public health, economics professor Aidan Hollis has proposed a solution in the form of user fees on the non-human use of antibiotics.

In a newly released paper published (closed science, sadly, so no link provide), Hollis and co-author Ziana Ahmed state that in the United States 80% of the antibiotics in the country are consumed in agriculture and aquaculture for the purpose of increasing food production.

This flood of antibiotics released into the environment – sprayed on fruit trees and fed to the likes of livestock, poultry and salmon, among other uses – has led bacteria to evolve, Hollis writes. Mounting evidence cited in the journal shows resistant pathogens are emerging in the wake of this veritable flood of antibiotics – resulting in an increase in bacteria that is immune to available treatments.

If the problem is left unchecked, this will create a health crisis on a global scale, Hollis says.

Hollis suggest that the predicament could be greatly alleviated by imposing a user fee on the non-human uses of antibiotics, similar to the way in which logging companies pay stumpage fees and oil companies pay royalties.

Bacteria that can effectively resist antibiotics will thrive, Hollis adds, reproducing rapidly and spreading in various ways.

“It’s not just the food we eat,” he says. “Bacteria is spread in the environment; it might wind up on a doorknob. You walk away with the bacteria on you and you share it with the next person you come into contact with. If you become infected with resistant bacteria, antibiotics won’t provide any relief.”

While the vast majority of antibiotic use has gone towards increasing productivity in agriculture, Hollis asserts that most of these applications are of “low value.”

“It’s about increasing the efficiency of food so you can reduce the amount of grain you feed the cattle,” says Hollis. “It’s about giving antibiotics to baby chicks because it reduces the likelihood that they’re going to get sick when you cram them together in unsanitary conditions.

“These methods are obviously profitable to the farmers, but that doesn’t mean it’s generating a huge benefit. In fact, the profitability is usually quite marginal.

“The real value of antibiotics is saving people from dying. Everything else is trivial.”

While banning the use of antibiotics in food production is challenging, establishing a user fee makes good sense, according to Hollis.

Such a practice would deter the low-value use of antibiotics, with higher costs encouraging farmers to improve their animal management methods and to adopt better substitutes for the drugs, such as vaccinations.

Hollis also suggests that an international treaty could ideally be imposed. “Resistant bacteria do not respect national borders,” he says. He adds that such a treaty might have a fair chance of attaining international compliance, as governments tend to be motivated by revenue collection.

Hollis notes that in the USA, a move has been made to control the non-human use of antibiotics, with the FDA recently seeking voluntary limits on the use of antibiotics for animal growth promotion on farms.

Discovered in 2005 by scientists from Bayer Healthcare in Germany, ADEP4 killed a variety of different bacteria and cured lethal infections in mice and rats.

Here’s how it works. Proteins need to fold into very precise shapes to do their jobs, and misfolded proteins are wastes of space. Bacteria dispose of these useless molecules with ClpP—a janitorial protein that digests other proteins. It works with a partner, which recognises misfolded proteins, unfolds them, and threads them through a hole in the middle of ClpP so they can be broken down. But ADEP4 opens ClpP up so it no longer needs its partner. The janitor now becomes an assassin, running amok and chopping up any protein it comes across, misfolded or not.

The Bayer scientists showed that ADEP4 can force fast-growing cells to self-destruct, but Lewis suspected that it would do the same to persisters. Afterall, ClpP’s partner requires energy to do its job, but ClpP itself doesn’t. Once ADEP4 opens it up, it should go about its fatal business even in a dormant cell.

Lewis’ team found that ADEP4 did effectively kills persister populations of Staphylococcus aureus, but the bacteria bounce back. ClpP isn’t essential, so the bacteria just inactivated it to evolve their way around ADEP4. This, says Lewis, is why Bayer stopped working on the drug.

His solution was to pair ADEP4 with another antibiotic called rifampycin. ADEP4 would kill off the majority of the persisters, and if any of the rest started growing again, rifampycin would finish them off. He predicted that the double-whammy would leave very few survivors, maybe just a thousand cells or so.

“That’s not what we saw,” he says. “What we saw was complete sterilisation.”

This is a very nice effort. As our efforts fail to find “magic bullet” antibiotics fail and antibiotic resistance increases combo drug solutions offer some hope. While this is good news, the overall state of our ability to treat bacterial infections continues to decline as our misuse of antibiotics has greatly increased the speed at which antibiotic resistance has developed in bacteria.

This solution only works on gram positive antibiotics. ADEP4 is too big to pass through the extra outer layers of the gram-negative bacteria like ecoli and salmonella.

we tend to (and especially those seeking to gain an advantage tend to – even if “we” overall wouldn’t the people in the position to take aggressive measures do) ignore risks until the problems are created (often huge costs at that point)

I think we should reduce risk and therefore make it hard to justify using GMO techniques

I agree the practice can be explained in a way that makes it seem like there is no (or nearly no) risk, I don’t trust we will always refrain from stepping into an area where there is a very bad result

Basically I would suggest being very cautious with GMO. I like science and technology but I think we often implement things poorly. I think we are not being cautious enough now, and should reduce the use of GMO to critical needs to society (patents on the practices need to be carefully studied and perhaps not permitted – the whole patent system is so broken now that it should be questioned at every turn).

The way we casually use drugs is another example of our failure to sensibly manage risks, in my opinion. This of course is greatly pushed by those making money on getting us to use more drugs – drug companies and doctors paid by those companies. The right drugs are wonderful. But powerful drugs almost always have powerful side effects (at least in a significant number of people) and those risks are multiplied the more we take (due to interactions, weakness created by one being overwhelmed by the next etc.). We should be much more cautious but again we show evidence of failing to act cautiously which adds to my concern for using GMO.

I love antibiotics, but the way we are using them is endangering millions of lives (that is a bad thing). I don’t trust us to use science wisely and safely. We need to more consciously put barriers in place to prevent us creating massively problems.

Untreatable and hard-to-treat infections from Carbapenem-resistant Enterobacteriaceae (CRE) germs are on the rise among patients in medical facilities. CRE germs have become resistant to all or nearly all the antibiotics we have today. Types of CRE include Klebsiella pneumoniae Carbapenemase (KPC) and New Delhi metallo-beta-lactamase (NDM). By following the United States Center for Disease Control (CDC) guidelines, we can slow the penetration of CRE infections in hospitals and other medical facilities and potentially spread to otherwise healthy people outside of medical facilities.

The CDC has worked with hospitals to successfully apply these measures. The CDC worked with Florida to stop a year-long CRE outbreak in a long-term acute care hospital. With the improved use of CDC recommendations (such as educating staff; dedicating staff, rooms, and equipment to patients with CRE; and improving use of gloves and gowns) the percentage of patients who got CRE at the facility dropped from 44% to 0.

Israel decreased CRE infection rates in all 27 of its hospitals by more than 70% in one year with a coordinated prevention program. The USA is at a critical time in which CRE infections could be controlled if addressed in a rapid, coordinated, and consistent effort by doctors, nurses, lab staff, medical facility leadership, health departments/states, policy makers, and the federal government.

As I have been saying for years the damage we are creating due to our actions around the use and abuse of antibiotics is likely to kill tens of thousands, or more people. Because the deaths are delayed and often not dramatic we have continued dangerous practices for years when we know better. It is a shame we are condemning so many to increased risks. The CDC, and others, are doing good work, unfortunately too much bad work is continuing in the face of evidence of how dangerous that is.